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CT scans remind me of luxury SUVs. 10 - 15 years ago, they were all the rage. Usher famously bumped up and down behind the wheel of a Navigator in his music video "You Don't Have to Call." It was an era when all the rappers cruised around in black-on-black SUVs with tinted windows and shiny spinning dubs as a testament to their masculinity and opulence. The general population followed in suit and the ozone took a debilitating blow. Not long after, Al Gore spearheaded a coup with a two hour-long keynote presentation, Morgan Spurlock got fat on "Supersize Me", and eventually the gas-guzzling urban assault vehicle craze of 2000 faded like the polluted cloud of smoke it left behind. A newly emerging Going-Green mentality began to spread and the clean-air technology electric car was the poster child for a new era.

I think I saw these in "Back to the Future"

To an enthusiastic emergency ultrasound fellow such as myself, I see a parallel trend in the field of emergency medicine. Patients today are becoming more concerned than ever about the irradiating doses of CT scanners. It seems fewer patients are willing to be injected with kidney-punching dyes and lay through a donut-shaped microwave just to reaffirm to them (us?) that the ungodly pain in their flank is, in fact, just a kidney stone.

A new horizon

A recent article in the New England Journal of Medicine brings to light a protocol utilizing point-of-care ultrasound to diagnose nephrolithiasis. In their multi-centered study they randomized 2759 patients into one of three groups: POC ultrasound performed an EP; ultrasound performed by a tech and read by a radiologist; and a traditional CT scan.

The authors described three primary outcomes--which, by the way, is sort of a misnomer. Studies really should only have one primary outcome and a bunch of secondary outcomes. Here, the main primary outcome was high-risk diagnoses with complications that could be related to missed or delayed diagnoses (AAA, appendicitis, cholecystitis, etc). Secondarily, the authors looked at things like complications rate, cumulative radiation exposure, cost, length of stay, readmissions, etc.

In a nutshell what they found was that aside from radiation exposure (POC U/S had the least), the three groups did not differ significantly on any of the measured outcomes.

Watch this 1-minute video by Mike and Matt of the Ultrasound Podcast demonstrate renal ultrasound.

Figure: demonstration of the increasing levels of hydronephrosis.

Mild Hydronephrosis

Moderate Hydronephrosis

Severe Hydronephrosis

Vicki Noble--an author in the NEJM article--illustrates an excellent protocol in her textbook Manual of Emergency and Critical Care Ultrasound. She proposes pairing a renal scan with an aorta scan. See an aorta ultrasound demonstration here.

The reasoning behind it is that for patients with renal colic pain is a consequence of complete or partial ureteral obstruction. Fluid will back up and results in mild to moderate hydronephrosis. Severe hyrdonephrosis is a bit more worrisome for a large, non-passable stone and may warrant further imaging with CT. Because AAA is a known mimicker of renal colic and disastrous when missed, a rapid aorta scan is essential, especially in patients older than 50.

To summarize, for patients presenting with flank pain or other symptoms concerning for renal colic you can attempt a bedside point-of-care work-up with ultrasound by scanning the kidneys, bladder, and aorta. I think "Sonographic Timely Assessment for Nephrolithiasis" is catchy, don't you?

I recently posted a 2-part entry on fluid dynamics and resuscitation (see here, and here), which described the use of bedside ultrasound as a guide to re-hydration therapy.

These posts contributed to the on-going debate regarding the utility of the IVC index and its relationship to right atrial pressures, which could be used as a “quick” or “dirty” measure of CVP and volume status when taken in the appropriate clinical context.

Probably not fluid responsive

Using an ultrasound “Triple Scan” of the heart, lung, and IVC to assess fluid responsiveness (i.e. an increase of cardiac output by 10-15% with small fluid challenge) seems like a reasonable surrogate to the highly impractical “gold medal” approach of calculating cardiac output using bedside ultrasound, performing a passive leg raise, and then re-calculating cardiac output.

Fluid Responsive

Using the right side of the heart to gauge fluid resuscitation works well for certain patients but it may carry inherent limitations for patients with a history of right heart failure, COPD, pulmonary hypertension, and other diseases with chronically elevated right-sided pressures. By using a pathologic right side (heart/ivc) as a measure, one that has a tendency for elevated pressures, we could potentially be misguided by a false sense of reassurance once achieving a non-collapsing IVC (“adequate preload”). To put it another way: how do we know—without actually measuring cardiac output—that optimizing the right heart with fluid equally benefits the left heart? Should we assume that the left ventricle can accommodate and push out the same supply of preload as the right? Are the left and right hearts equal?

In my original posts I proposed having a quick peek at the lungs for the presence of interstitial edema (B-line predominance) and at the left ventricular squeeze to assess whether adding volume would benefit (heart is fluid responsive, on the up-sloping phase of Frank-Starling’s curve) or overwhelm the heart and result in pulmonary edema (plateau phase of the Frank-Starling curve). However, these are qualitative visual estimates and are not entirely accurate.

Diastology is the study of the heart’s ability to relax and comply (stretch) with preload volume. If the ventricle is impaired or restricted, it cannot accept the volume we give it and therefore will not be responsive to added fluid. Therefore, if there is underlying moderate to severe left ventricular diastolic dysfunction, gauging our efforts of fluid resuscitation from the right heart is potentially misleading:

In a diastolic dysfunctional LV with normal RV, bulking up the IVC and RA pressures could potentially overwhelm the LV

In a diastolic normal functional LV with chronically elevated RA pressures, there is potential for under-resuscitation of the left heart

Perhaps then it may benefit us to take a closer look at LV function when gauging the adequacy of our initial fluid loading…

Here’s how to do it:

Obtain a 4-chamber apical view. If it’s poorly visible, try rolling the patient into the left lateral decubitus position. If still not obtainable (or rolling is not feasible), stick to heart/lung/IVC as your guide.

Measure the mitral valve inflow velocity [MVI] (how fast blood rushes in to the left ventricle during diastole) by placing a doppler gate over the superior end of the mitral valve leaflets as they open. The result will show a series of two-wave pattern representing Early diastolic filling (E wave) and atrial kick (A wave) in late diastole. The magnitude and ratio of these two waves represents normal to abnormal filling (diastolic dysfunction).

Next, shift your doppler gate over to the superior-most portion of the inter ventricular septum adjacent to the mitral valve annulus. Turn “TDI on” to get a Tissue Doppler measurement of how fast and how much the septum in this region elongates as blood rushes into the ventricle and stretches it during diastole. The result will show again a two-wave pattern in series, this time upside down (since annulus shoots toward bottom of screen as it stretches during filling). The e’ wave and a’ prime wave correspond temporally with the E and A waves seen prior and their ratios and magnitudes also help determine normal from abnormal filling (diastolic dysfunction).

Here's a summary chart:

“Shortcuts”: You may notice that if you see an E velocity value < 100 and its size is greater than the A wave, you’re done (it’s normal).

You many also notice that if the e’ velocity is > 8 cm/s in TDI, you’re done (it’s normal).

If A > E, it is impaired function.

My take on this is if a patient continues to be in a state of hypo perfusion or hypotension and the IVC no longer collapses (low IVC index), I look at the lungs and heart.

If the LV diastolic function is normal, even impaired, I may add more volume to bring that patient toward pseudo normal relaxation. At this point, any further efforts at increasing perfusion would be directed at pressors/inotropes knowing that the heart has reached its limit of fluid responsiveness.

While the latter study remains a bit cavalier to most US-based emergency physicians it offers hope and promise that ultrasound, when combined with a good history and physical exam and, when warranted, lab data can prevent unnecessary use of radiation, admissions, antibiotics (empiric), and painful procedures.

A good approach may be:

History and physical exam followed by bedside ultrasound

No effusion and reassuring (minimal Kocher present) clinically?

close follow-up with NSAIDs

Concerning clinically (> 2-3 Kocher or strong suspicion based on H+P) with effusion

M.S. Kocher, D. Zurakowski, and J.R. Kasser, "Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm.", The Journal of bone and joint surgery. American volume, 1999.

S.J. Luhmann, A. Jones, M. Schootman, J.E. Gordon, P.L. Schoenecker, and J.D. Luhmann, "Differentiation between septic arthritis and transient synovitis of the hip in children with clinical prediction algorithms.", The Journal of bone and joint surgery. American volume, 2004

M.M. Zamzam, "The role of ultrasound in differentiating septic arthritis from transient synovitis of the hip in children.", Journal of pediatric orthopedics. Part B, 2006.

Rivers produced an elegant (now slightly outmoded) algorithm for resuscitating septic patients. It begins by filling the tank (initial 20 cc/kg of fluid) and then, if still hypotensive, dropping a central line and titrating fluid boluses to a CVP of 8-12 mmHg. At that point pressors become an option for elevating MAP and improving peripheral perfusion.

CVP, unless extremely low (0-2 mmHg), is no longer considered a valid marker of fluid status--it only indicates RA pressure.

Ultrasound measurement of IVC diameter fluctuance with respirations is a better correlate to a patient's volume status

And so here we are. You checked the IVC, you bolused your patient. The IVC now shows minimal fluctuation. Hurray! Hold the celebration Shlomo; the patient is still hypotensive and poorly perfusing.

Is this full septic shock? Are pressors be the right call? Maybe we still need to give more fluid first? More importantly, if we do give more fluid, will it help to improve cardiac output (and in turn increase perfusion and MAP) or will it just back up and lead to ARDS and pulmonary edema?

Before addressing these conundrums, we must first revisit a simple concept that Guyton outlined decades ago. I'm talking of course about the Frank-Starling curve of cardiac function.

"Learn it, no pressure. ZING! See what I did there?"

Patients who have a PMH of CHF or ESRD may be on the low end of the curve, but would that preclude them receiving fluid? This is a common pitfall for many resuscitationists who fear iatrogenic pulmonary edema and fall short of adequately repleting these patients.

On the other end, sepsis and acidotic states can induce cardiac dysfunction in patients without previous cardiac insufficiency.

Measuring CVP or looking at IVC diameter is a reflection of preload to the right heart in static and dynamic terms, respectively. It says nothing of the left heart or its ability to pump more volume forward if given the opportunity with more fluid. The patient, therefore, may lie at any point along the graph. But which slope they occupy would otherwise remain a mystery.

Left heart is the dark side of the moon.

The topic surfacing here is the concept of fluid responsiveness: that increasing volume leads to an increase in cardiac output. Patients on a low slope of the F-S curve have minimal if any room to increase contractility with added volume, whereas healthier hearts maintain an ability to increase contractility to greater extents when more and more volume is added.

Mike and Matt go one step further and assess the actual cardiac response to a small fluid bolus that is fully reversible (passive leg raising)--visualizing the F-S response. To assess whether your patient is a responder--that is, with added bolus the cardiac output increases by 5-10%, you would have to perform a complex set of measurements to arrive at the CO. Even though this is the most validated and thorough approach (the "gold medal") it comes at the cost of more calculations, operator skills, time consumption, and holding a pair of legs in the air for 2 minutes.

Consolidating the above I propose a simple, rapid, etiology-driven approach to resuscitating your sick and septic patients with the aid of an ultrasound - a way to decide which patients need more fluid and which will no longer benefit (no positive response)

It all starts with the IVC: if it collapses > 50% with each breath (or distends > 18% with each mechanical breath), your patient--with very high certainty--needs volume. -When the IVC no longer shows dramatic fluctuation, a benefit from additional fluid is dubious. In some it may cause harm, overwhelming the myocardium leading to back flow (the patient on a lower F-S slope).

Near 100% collapse. Better give fluid.

Fully distended. Need to check left heart.

At this point we scan the heart. A detailed echo is not necessary; just one view qualitatively checking for LV systolic function (is the LV hyper dynamic with kissing walls or is it severely dilated with poor contractility?) can provide you with the information needed in less than 15 seconds.

Dilated LV, poor systolic function.

If the left heart appears to be contracting well, an additional bolus may very well increase cardiac output--the patient is fluid responsive (or at least tolerant).

If the heart appears overloaded, with poor systolic function proceed to a quick scan of the lungs. Numerous B lines, as in pulmonary edema, indicate that this patient occupies a lower slope along the Frank-Starling graph (poor cardiac function) and would likely not respond well (cannot tolerate) to additional volume. In this scenario, initiation of vasopressors to increase output and MAP would be more appropriate.

Thanks Medscape!

If the lungs defy expectations and appear rather clear (no greater than 3-4 B lines per intercostal field) than this patient may still be fluid tolerant and accommodate an additional small fluid bolus.

It's been nearly 13 years since the publication of the landmark Rivers early goal directed therapy study in the NEJM. As with a Bar Mitzvah, the Jewish rite of passage from youth to manhood, it's now time for EGDT's transformation and to face post-pubescent changes that go hand-in-hand with maturity, development, and the right to start drinking Maneschwitz. The developments I allude to here are reflections of the various (improved, more accurate) modalities many of us now use to detect the different goal posts set out in Rivers' algorithmic approach to severe sepsis. Let's explore this growth together.

First, consider a case scenario:

A 66 year old female (history of diabetes, hypertension, CHF) from home presents with fever and productive cough with the vitals: BP 88/50, HR 120, RR 20, T 39 C. She is confused and has dark urine.

You place her on a monitor, insert a foley catheter, add supplemental oxygen via nasal cannula, and place an IV to send labs and administer an initial bolus of 20-30 cc/kg of crystalloid fluid. Antibiotics are running in the IV. 15 -20 minutes later, she is still hypotensive. Do you give more fluid? Or do you now place a central line and add pressors (like norepinephrine)?

In the original Rivers model, once the presence of severe sepsis/septic shock is recognized and the decision is made to proceed with EGDTto guide us in reaching the ultimate point in a severely septic patient--normalize tissue perfusion--we will first and foremost satisfy the most important goal of "filling up the tank" completely and adequately with IV fluid. Only then can we begin moving further to subsequent potential deficiencies/goals that demand addressing: "tightening the pipes" (MAP > 65 with pressors), "optimizing the pump" (optimize cardiac output with inotropy), and "adding passengers" (transfusion of blood product to increase oxygen carrying capacity). With each subsequent step, you keep going back to check and see if you've met your ultimate goal of improved tissue perfusion/oxygenation by looking to surrogate marker of perfusion: ScvO2 (Rivers) or, in the 2008 Jones non-invasive model, serum lactate clearance.

Here's the algorithm:

For a more detailed explanation of the above analogy on tank/pipes/pump/and passengers, see the previous blog post on water slide physiology.

We kosher so far? Good. Let's move along.

The meat of this discussion and important question to ask yourself next is "have I really given enough fluid? Was the initial crystalloid bolus adequate for volume repletion or does the patient still require more to meet the primary goal of filling up the tank?" Rivers' answered this dilemma by dropping a central line in all his patients and measuring the CVP: if it was less than 8-12 mmHg, he gave more fluid until the goal pressure (8-12) was achieved. If CVP was eventually optimized to 8-12 mmHg ('an adequate preload') and the patient was still hypotensive, he'd move down the chain and begin pressors to address the MAP ('optimize afterload'). (See above figure). The assumption here of course is that CVP is a good marker of a patient's fluid status--a fuel tank gauge on the physiologic dashboard, if you will.

Today we know that isn't true. There are two huge shortcomings to this approach:

With the risk of giving too little or too much fluid and increasing the morbidity/mortality, we welcome a better, more accurate evolutionary approach to detecting a patient's volume status at the bedside...

Ultrasound! What else??

There is now sufficient data to support the use of ultrasound-based measurement of IVC diameter fluctuation during the respiratory cycle in order to gauge volume status. (EMCrit reviews them here). The background concept is quite simple:

-In a volume depleted spontaneously breathing patient: each breath lowers intrathoracic pressure, which in turn increases cardiac return (like a suction pump). As the already low reserve of intravascular volume is shifted up into the chest with each inspiration, the highly-compliant IVC will collapse.

(ignore the bit about a sniff test)

Balloon is the IVC, collapsed with sucked-out volume

-In a volume depleted mechanically ventilated patient: each administered breath from the vent increases intrathoracic pressure, which in turn lowers cardiac return and pushes blood back down into the abdomen (like a piston). The depleted IVC, now receiving an inspiratory surge of volume, will noticeably distend.

Man is the ventilator; balloon is IVC

Most of the papers validating the use of IVC ultrasound are based on mechanically ventilated patients, since tidal volume is set and each breath is controlled, The literature is not as clear for spontaneously breathing patients due to an inherent variability with each breath taken. These are the patients we care for more frequently though and for obvious reasons we prefer to use a less invasive approach to fluid monitoring when possible.

That's ok.

There is good news however; research does agree with good consistency and relatively high specificity that on the lowest extreme of the fluid status spectrum--volume depletion--grossly (easily) visible IVC collapse (of greater than 40%) on B-mode sonography is suggestive of a fluid depleted state where patients will benefit from further volume resuscitation. As Weingart puts it: "if you see it collapse give more fluid, if you see it collapse give more fluid, if you see it collapse give more fluid!"

At this point we're beginning to run long, so I'm going to take a much-needed pause here. We will resume our discussion in part II, where I'll be addressing the pressing concern of how to determine if your patient requires more fluid therapy if or when the IVC does NOT show obvious fluctuation with respirations (>40% collapse in spontaneously breathing and <18% dissension in mechanically ventilated patients). This is the scenario, unfortunately, that we are more likely to encounter--"the gray zone" as it were--while working up septic patients--especially if checking the IVC after an initial bolus. In other words, just because it's not collapsing (distending in MV patients) does it imply they no longer need IVF, that the tank is completely full? Be sure to check back in soon for the explanations and illustrations.

I was recently playing and swimming with my 2 year old nephew at the local pool. This particular pool had a water slide. As we splashed around blissfully and took our turns shooting out from the green tubing I realized something: basic physiology and critical care pathophysiology can be simplified into a water slide model. To understand the basic mechanics of the water slide is to understand the basic principles of treatment of the septic patient, as in Rivers' early goal directed therapy.

The components of a typical water slide are:

pump

water

slide/tube

people!

Vessels in the body, like the tube of the water slide, transport blood and plasma (people and the water) to the systemic circulation of the body (the swimming pool). Then a long stem pipe (IVC) carries fluid back up to the top of the tower via a pressure gradient generated by a large water pump (the heart). The people, like red blood cells, carry excitement (oxygen) as they begin at the top and prepare for descent. On the way down, they let out a gleeful cry until reaching the bottom and, like the water in the system, emerge from its depths and make their way back up to the top--but using stairs instead of the water pipe of course.

Make sense? Good. Now let's see what can go wrong with the system and how we repair it.

Drained pool, no water -- the volume depleted patient

Without water the tube has no lubrication to facilitate the passage of people (cells, contents) from the tower down the tube (vessels) and into the pool (body). Septic patients are generally fluid depleted and lack proper perfusion to tissues, unable to bring oxygen-rich RBCs to the body. They therefore require initial fluid repletion as an initial modality of their resuscitation [how much fluid and how to gauge their response to fluid therapy will be covered in a future post]. The above concept has been summarized in various podcasts and described as "filling the tank."

If the water slide has a broken tube or large cracks and gaps in the tube, water would leak through its pores or, worse yet, people may get stuck in the misshaped apparatus. To be fully functional, the actual tube would require tightening and readjustment in order to once again allow safe and efficient passage of people down the slide. In the same vein (pun intended), septic patients who are persistently hypotensive often require vasopressor therapy to facilitate organ tissue perfusion once initial volume (fluid) repletion is assured. In the past, this has been referred to as "fixing or tightening the pipes."

3. Pump failure -- poor cardiac output/cardiac dysfunction

Without a properly functional pump generating enough force and pressure to bring water from the bottom of the pool back up to the top of the slide, the system will fail and people can no longer be properly shuttled. Analogous to the above scenario poor cardiac output secondary to cardiac dysfunction and poor cardiac contractility demonstrates the same type of deficiency. We often observe this in septic patients who require require inotropic agents to optimize their cardiac output, whether determined by direct observation of the heart using an ultrasound (preferable) or once volume and and vessels are corrected (steps 1 and 2 above) and a shock state remains. This is commonly referred to as "fix the pump."

4. No people or a lack of excitement -- anemia, hypoxemia

It's simple: if there's a water slide, but no one there to go ride it, does it even exist? Similarly, if people are present but apathetic about the slide, will anyone ride? To make the analogy, people--previously described as red blood cells--are essential to a successful water slide system. They carry excitement and glee (oxygen). If they are missing--as in a state of anemia--or are apathetic and cannot be excited (hypoxemia) the system is again broken. We must either replace missing people (transfusion of packed RBCs) or rile them up (provide oxygen whether by face mask, nasal cannula, or mechanical ventilation).

Following these steps along the analogy's path essentially covers the basic tenants of severe sepsis, shock, and the concept behind correcting the broken physiology of such patients, as described in 2001 by Manny Rivers and all those who followed.